Of mice and men: more neurobiology in dementia
- 1 November 2006
- journal article
- review article
- Published by Wolters Kluwer Health in Current Opinion in Psychiatry
- Vol. 19 (6) , 555-563
- https://doi.org/10.1097/01.yco.0000245757.06374.6a
Abstract
An increasing number of genetically modified mouse models are designed and used in the field of Alzheimer disease research. This review aims to offer a general view of the existing transgenic mouse lines and to discuss their relevance and limitations. Potential therapeutic targets have been identified in rodent models of Alzheimer disease. Although important steps towards obtaining a safe vaccine to prevent amyloid plaque formation have been made, further evaluations and the use of intermediate models are considered a necessity. More than 18 million people worldwide are suffering from Alzheimer disease, the most common dementing disorder in humans. Transgenic lines have been created in order to understand the underlying mechanisms of Alzheimer disease and to find a cure. None of the available models completely recapitulates the characteristics of human pathology, but they provide valuable information on different pathogenic pathways involved. New therapeutic approaches and improvement of current strategies can be obtained from the use of Alzheimer animal models.Keywords
This publication has 98 references indexed in Scilit:
- Alzheimer's disease-like neuropathology of gene-targeted APP-SLxPS1mut mice expressing the amyloid precursor protein at endogenous levelsNeurobiology of Disease, 2005
- Preserved Fronto-Striatal Plasticity and Enhanced Procedural Learning in a Transgenic Mouse Model of Alzheimer's Disease Overexpressing MutanthAPPsweLearning & Memory, 2004
- Interleukin-6 promoter polymorphism: risk and pathology of Alzheimer's diseaseNeuroscience Letters, 2004
- Genetic association of Alzheimer's disease with multiple polymorphisms in alpha-2-macroglobulinHuman Molecular Genetics, 2003
- The 'Arctic' APP mutation (E693G) causes Alzheimer's disease by enhanced Aβ protofibril formationNature Neuroscience, 2001
- Selective vulnerability of neocortical association areas in Alzheimer's diseaseMicroscopy Research and Technique, 1998
- Tau is a candidate gene for chromosome 17 frontotemporal dementiaAnnals of Neurology, 1998
- Increased amyloid beta-peptide deposition in cerebral cortex as a consequence of apolipoprotein E genotype in late-onset Alzheimer disease.Proceedings of the National Academy of Sciences, 1993
- Neuropathological stageing of Alzheimer-related changesActa Neuropathologica, 1991
- Segregation of a missense mutation in the amyloid precursor protein gene with familial Alzheimer's diseaseNature, 1991